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Alterations of T‐cell surface markers in older women with persistent human papillomavirus infection
Author(s) -
Rodríguez Ana Cecilia,
GarcíaPiñeres Alfonso J.,
Hildesheim Allan,
Herrero Rolando,
Trivett Matthew,
Williams Marcus,
Atmella Ivannia,
Ramírez Margarita,
Villegas Maricela,
Schiffman Mark,
Burk Robert,
Freer Enrique,
Bonilla José,
Bratti Concepción,
Pinto Ligia A.
Publication year - 2010
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.25371
Subject(s) - peripheral blood mononuclear cell , hpv infection , cd8 , immunology , population , lymphocyte , genotyping , medicine , immune system , cohort , flow cytometry , genotype , biology , cervical cancer , cancer , genetics , environmental health , gene , in vitro
We previously reported decreased lymphocyte proliferative responses among older women with persistent human papillomavirus (HPV) infection. To characterize the phenotype of peripheral lymphocytes associated with persistent HPV infection, we evaluated the expression of different cell surface markers in peripheral blood mononuclear cells (PBMCs) from a case–control study within a 10,049 woman population‐based cohort study in Guanacaste, Costa Rica. Women in the cohort aged 46–74 and with HPV results at their 5th year anniversary visit were considered, and all women ( n = 87) with persistent HPV infections, all women ( n = 196) with transient HPV infections and a random sample of HPV DNA‐negative women ( n = 261) frequency‐matched to cases on age were selected for this study. A median of 3 years after the case–control matching visit, cervical cells were collected for liquid‐based cytology and repeat HPV DNA genotyping. Blood was obtained from which PBMCs were extracted and cryopreserved for immunological phenotyping via flow cytometry. Significant increases in risk of HPV persistence were observed for 3 marker subsets indicative of immune cell activation/differentiation. Relative risk estimates were 5.4 (95% CI = 2.2–13.3) for CD69 + CD4 + , 2.6 (95% CI = 1.2–5.9) for HLADR + CD3 + CD4 + and 2.3 (95% CI = 1.1–4.7) for CD45RO + CD27 − CD8 + . A significant decrease in HPV persistence was observed for a subset marker indicative of an immature, undifferentiated memory state CD45RO + CD27 + CD4 + (OR = 0.36; 95% CI = 0.17–0.76). Adjustment for these markers only partially explained the previously reported association between decreased lymphoproliferative responses and persistent HPV infection. Whether phenotypic alterations observed predispose to HPV persistence or result from it should be the focus of future studies.